Fig. 3

Genomic landscape of G0 arrest decisions in cancer. a Cancer drivers with mutations or copy number alterations depleted pan-cancer in a G0 arrest context. Features further selected by the pan-cancer model are highlighted. b Schematic of the ensemble elastic net modelling employed to prioritise genomic changes associated with G0 arrest. c Genomic events significantly associated with G0 arrest, ranked according to their importance in the model (highest to lowest). Each point depicts an individual tumour sample, coloured by the value of the respective feature. For discrete variables, purple indicates the presence of the feature and green its absence. The Shapley values indicate the impact of individual feature values on the G0 arrest score prediction. d G0 arrest levels are significantly reduced in microsatellite unstable (MSI) samples in stomach adenocarcinoma (STAD) and uterine corpus endometrial carcinoma (UCEC), with the same trend (albeit not significant) shown in colon adenocarcinoma (COAD). Wilcoxon rank-sum test *p < 0.05; **p < 0.01. e Genomic alterations are depleted across DNA repair pathways during G0 arrest. Odds ratios of mutational load on pathway in G0 arrest are depicted, along with confidence intervals. CS, chromosome segregation; p53, p53 pathway; UR, ubiquitylation response; CPF, checkpoint factors; TM, telomere maintenance; CR, chromatin remodelling; TLS, translesion synthesis; NHEJ, non-homologous end joining; NER, nucleotide excision repair; MMR, mismatch repair; FA, Fanconi Anaemia; BER, base excision repair. f G0 arrest scores are increased in cell lines with slow doubling time across MCF7 strains, which also show lower prevalence of PTEN mutations. g Tissue-specific changes in G0 arrest between samples with/without quiescence-associated deletions (blue), amplifications (red) and SNVs (brown) within the TCGA cohort (top) and external validation datasets (bottom)